Epidemiological characteristics of eczema and the global burden of disease network

Rodriguez, Ramiro; Dellavalle, Robert P.

doi:10.1111/cea.14287

Cited by 1 publication

(2 citation statements)

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“…In China, AD affects 6.13% of adults, 12.94% of children aged 1–7 years and 40.81% of infants aged 3 months 5–7 . The clinical symptoms of AD generally manifest as itching, dry skin and rash, which can influence the quality of life of patients and result in a heavy financial burden for patients’ families, particularly with the increasing severity of the disease 8 . Genetic and environmental factors both contribute to the incidence of AD 1,9 .…”

Section: Introductionmentioning

confidence: 99%

“…the disease. 8 Genetic and environmental factors both contribute to the incidence of AD. 1,9 Despite an incomplete understanding of the pathogenesis of AD, several mechanisms, including heredity, environmental factors, impaired skin barrier, immunological defects, oxidative stress and microbial dysregulation, are known to be involved in the progression and development of AD.…”

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confidence: 99%

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Esculentoside A ameliorates DNCB‐induced atopic dermatitis by suppressing the ROS‐NLRP3 axis via activating the Nrf2 pathway

Liu

Liao

2023

Clin Exp Pharma Physio

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Atopic dermatitis (AD) is a chronic inflammatory skin condition with a high prevalence. Inflammation and oxidative stress are strongly associated with AD progression. Esculentoside A (EsA) inhibits inflammation and oxidative stress in various diseases. However, whether EsA mitigates AD by suppressing inflammation and oxidative stress remains unknown. A mouse model of AD was constructed by the induction of 1‐chloro‐2,4‐dinitrochlorobenzene (DNCB). The mechanism of EsA and its effects on AD symptoms, pathology, inflammation and oxidative stress were investigated through histopathological staining, enzyme‐linked immunosorbent assay, blood cells analysis, colorimetric measurement and western blot analysis. EsA improved the clinical symptoms and increased clinical skin scores in AD mice. Skin thickening of the epidermis and dermal tissues and the mast cell numbers in AD mice were reduced with the EsA treatment. EsA decreased the relative mRNA level of thymic stromal lymphopoietin, interleukin (IL)‐4, IL‐5 and IL‐13; the serum concentrations of immunoglobulin E (IgE) and IL‐6; and the numbers of white blood cells (WBC) and WBC subtypes, including basophil, lymphocytes, eosinophil, neutrophil and monocytes in DNCB‐induced mice. DNCB caused higher levels of oxidative stress, which was reversed with the administration of EsA. Mechanically, EsA upregulated the expression of Nrf2 but downregulated the level of NLRP3 inflammasome in AD mice. The inhibitor of Nrf2 significantly recovered the EsA‐induced changes in the NLRP3 inflammasome proteins in DNCB‐treated mice. Therefore, EsA improved the clinical and pathological symptoms, inflammation and oxidative stress experienced by DNCB‐induced mice and was involved in the inactivation of NLRP3 inflammasome by activating Nrf2.

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Section: Introductionmentioning

confidence: 99%

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confidence: 99%